Soybean cyst nematode causes more than one billion dollars in annual yield losses to US soybean producers and is a continuing problem in soybean producing regions throughout the world. Virulent populations of Heterodera glycines, the nematode responsible for this yield loss, have been identified on most known resistance sources. But the soybean genes which confer resistance to soybean cyst nematode have not been previously cloned.
Cyst nematodes belonging to genera Heterodera and Globodera include some of the most economically important classes of plant-parasitic nematodes. Different species of these nematodes feed selectively on certain host plants as obligate sedentary endoparasites by inducing specialized feedings sites (syncytia) within host roots. The soybean cyst nematode (SCN) Heterodera glycines Ichinohe has a host range limited to plants in the family Leguminosae and some weeds. It is consistently the most economically important pathogen on soybean (Glycine max (L.) Merr.) (Koenning and Wrather, 2010). Infective second-stage juveniles (J2) hatch from eggs in the soil and penetrate plant roots utilizing a hollow mouth spear (stylet) to mechanically perforate the plant cell wall and to secrete cell wall digesting enzymes that facilitate intracellular migration through the root cortex to a pericycle or endodermal cell near the vasculature. Once a cell has been selected for feeding, the nematode delivers a suite of effector proteins into the cell leading to its transformation into a unique, highly metabolically active feeding cell. The now sedentary juvenile feeds from this cell as it progresses through a 25-30 day life cycle divided into four juvenile (J1-J4) and the sexually dimorphic adult life stages. After fertilization by a male, the adult female retains hundreds of eggs in her uterus and following her death forms a protective cyst that allows the eggs to survive for years in the soil in the absence of a host. The host plant suffers from loss of nutrients and reduced transport through the vasculature, manifested as less vigorous growth and reduced yield.
Its amphimictic lifestyle and unique survival strategy complicate current measures to control SCN. The use of nematicides is restricted and not cost-effective for soybean producers. Current methods to control SCN include a combination of nonhost crop rotation and planting of resistant cultivars. Soybean breeders have been successful in developing SCN resistant cultivars. The first Rhg (for resistance to Heterodera glycines) genes were identified in the early 1960's (Caldwell et al., 1960; Matson and Williams, 1965) and since then numerous papers on the identification and localization of QTL (quantitative trait loci) underlying resistance to SCN from a variety of different germplasm sources have been published. QTL on chromosome 18 (rhg1) and chromosome 8 (Rhg4) have been consistently mapped in a variety of germplasm sources (Concibido et al., 2004). In some sources, such as PI88788, rhg1 is sufficient for full resistance and displays incomplete dominance (Concibido et al., 2004). In other cases, such as the soybean cultivar (cv.) Forrest, full resistance to SCN requires both rhg1 and Rhg4, with Rhg4 exhibiting dominant gene action (Meksem et al., 2001).
Plants carrying Rhg genes display an incompatible interaction between host and parasite. The roots of plants carrying Rhg genes are penetrated by infective J2s, but feeding cells ultimately degenerate and most of the nematodes die before reaching adult stages (Endo, 1965; Riggs et al., 1973). Genetic variability in H. glycines is prevalent and nematodes that survive on resistant cultivars carry the undefined ror (reproduction on a resistant host) alleles (Dong and Opperman, 1997) leading to population shifts in the field as a consequence of soybean resistance monoculture (Niblack et al., 2008). Understanding of resistance to SCN is limited because the genes underlying identified SCN resistance QTL have not been cloned (Melito et al., 2010; Liu et al., 2010).